8.3.1  Exudative Age-Related

Macular Degeneration

In general, active leakage from a CNV will result in fluid accumulation beneath and within the neuroretina [31]. Visual function in macular edema, however, depends on the integrity of the retinal photoreceptor layer [32]. In NIR imaging, the increased fluid content at the posterior pole amplifies the near-infrared light absorption and scattering [17]. As a result, less light will reach the camera detector, causing regions with increased fluid exudation to appear darker on the NIR image [33]. This reduced photoreceptor reflectivity in NIR in patients with macular edema is directly related to the severity of edema [34]. The area of leakage and edema on the fluorescein angiogram corresponds to a dark, poorly defined halo around the CNV lesion on NIR imaging (Fig. 8.4). We will now discuss the appearance of various types of CNV in AMD on the NIR image. The entity of IPCV will be discussed separately in the following section.

8.3.1.1  Classic Choroidal Neovascularization

Before the introduction of anti-VEGF treatment of neovascular AMD, only classic CNV cases with well-defined borders were applicable for treatment by either focal laser coagulation or photodynamic therapy [35, 36]. Classic cases show high blood flow within the lesion and are surrounded by a characteristic pigmented halo [4, 37]. These features account for the characteristic findings on NIR imaging of classic CNVs [19, 38].

Classic CNVs are typically located anterior to the RPE [4] and therefore only little NIR light reflection and

absorbance occurs, which accounts for a good visibility of the classic CNV lesion in the near-infrared. A main attribute of classic CNV lesions in NIR appearance is the combination of a central dark core surrounded by a bright corona (Fig. 8.5). The ring-shaped bright corona may be incomplete in up to one-third of the cases [19]. The active neovascular process is depicted as a dark core due to the bloodand fluid-related light absorption in this area.

It has been shown that neovascular changes due to AMD may not only lead to hypertrophic RPE reactions, but also to exudation of fibrin in the area adjacent to the CNV [6, 39]. More so than melanin, fibrin is a relatively strong reflector in the near-infrared [29]. The bright nimbus surrounding the classic membranes is only partially co-located with the funduscopically visible pigmented halo. Hence, the bright corona on NIR imaging of classic CNV lesions may probably reflect not only the hypertrophic RPE reaction, but also the fibrin exudation.

8.3.1.2  Occult Choroidal Neovascularization

The occult form of CNV is the most frequent neovascular lesion type in AMD [40]. On fluorescein angiogram, occult CNVs are typically characterized by the phrase “late leakage of undetermined source”; however, they may appear as shallow fibrovascular detachments when examined by OCT. Based on the exact anatomical position of the membrane, light reflection, scattering, and absorption all add to the near-infrared image [27]. Contrary to classic lesions, occult neovascular membranes are poorly demarked and show overlying scattered NIR increase (Fig. 8.6). With regard to histology, occult

CNV membranes are largely located posterior to the RPE [1, 2]. On the surface of the occult CNV, disseminated fibrin coagulates have been found [6], which may be related to the spotted NIR increase. Frequently observed alterations of the RPE and small drusen in occult CNV cases may also add to their NIR appearance. RPE loss, for instance, will cause increased choroidal reflectivity and drusen may decrease NIR focally.

8.3.1.3Vascularized Detachment

of the Retinal Pigment Epithelium

If fluid is trapped beneath the RPE, an occult CNV may cause a dome-shaped RPE detachment, despite slow vessel proliferation and only mild leakage. Typically, a peripheral hyperfluorescent notch on fluorescein angiography suggests the presence of a CNV associated with such an RPE detachment [37]. The optical appearance of an RPE detachment on NIR is determined by its anatomical contour, melanin content, and turbidity of

the sub-RPE fluid. In addition, the appearance of the lesion is largely determined by the focus of the SLO [41]. If the focal plane of the image is near the apex of the RPE elevation, then the lesion appears bright due to the light scattered by the pigment epithelium. However, if the image is focused deep to Bruch’s membrane, a dark core caused by light absorption within the turbid sub-RPE fluid will dominate the lesion center. The edges of the RPE elevation will appear bright due to the oblique position and associated scattering of the incoming light. This summation of melanin reflectance and light scattering results in a strong NIR signal. Usually, a thin dark halo caused by a discrete serous retinal elevation surrounds the RPE detachment (Fig. 8.7). In general, an RPE detachment will appear as round lesion with a centrally decreased reflectivity by turbid subRPE fluid, delimited by a thin, brighter nimbus and bordered by a dark, irregular halo [42]. As in occult lesions without RPE detachment, the CNV membrane is poorly defined.

8.3.1.4  Mixed-Type Choroidal Neovascularization

In a minority of cases, a nonuniform type of CNV will occur [43]. In fluorescein angiography, these membranes are classified into minimal classic and predominantly classic CNV lesions. In NIR, these mixed types show characteristics of both classic and occult CNVs (Fig. 8.8). As in fluorescein angiography, the lesion type may be

estimated by the area covered by the classic and occult portion, respectively.

8.3.1.5  Retinal Angiomatous Proliferation

Unlike regular exudative AMD, the neovascular membrane in retinal angiomatous proliferation (RAP) originates from the neuroretina [44]. The formation of a CNV

in RAP is therefore an inherently secondary process. Once the CNV has formed, the differentiation between non-RAP and RAP lesions on NIR may become impossible. The neovascular membrane in the early pre-CNV stages of RAP, on the other hand, may show unique optical properties. In these early RAP cases, focally increased

NIR signals within a darkened, ill-defined area can be observed (Fig. 8.9). This hyperreflection is most likely associated with the fibrinous material located within the edematous swollen retina surrounding the lesion, as demonstrated in the histological preparations of RAP patients [39]. Interestingly, some RAP cases show a much

larger zone of decreased NIR than is to be expected from the corresponding fluorescein angiogram. This may be caused by abnormalities in the Müller cell population,

resulting in an increase in the NIR light absorption prior to macroscopic thickening of the neuroretina or leakage on the fluorescein angiogram [45, 46].